Intimal and neointimal fibroplasia leading to late failures of at least 50% of arterial reconstructions have been extensively documented, bear striking resemblance to atherosclerosis obliterans, and appear to be hemodynamically dependent. Based upon clinical observations in failed arterial reconstructions, experimental models have been developed in dogs by alteration of local hemodynamic conditions and extensively studied by light and electron microscopy for serial changes. Having standardized a number of hemodynamic models, it is planned to perfuse these models in situ with a variety of fluids to learn the role of various components of blood in the development of lesions. The specific stimuli which result in smooth muscle cell migrations may thereby be determined. The role of mitotic division in the development of fibromuscular intimal plaque has been studied by continued use of antimitotic drugs such as colchicine and cell counting at various stages of evolution of the plaques in arterial autographs and in endarterectomized segments. The relationship of fibrous intimal plaques to compound atherosclerosis is being studied by alteration of lipid profiles in animals with various hemodynamic models. In addition, the cellular mechanisms by which the arterial wall heals after endarterectomy and the effects of hemodynamic alterations on these mechanisms have been studied.